CHAPTER 42 The Effects of Training on Echocardiographic Measurements
The heart has a unique capacity for adapting to altered loading conditions. In the face of increased physical demands, the heart increases the volume of blood pumped by increasing stroke volume and heart rate. For short-term needs, the heart can cope with the greater volume or pressure loads. However, when the overload is sustained over time, such as during exercise, left ventricular (LV) hypertrophy (i.e., an increase in LV muscle mass) develops. Left ventricular hypertrophy is a physiologic phenomenon described in human and equine athletes as “athlete’s heart.” Pathologic LV hypertrophy can be induced by chronic hypertension and cardiac valvular disease and the ensuing pressure overload. Pathologic LV hypertrophy is distinguished from physiologic cardiac hypertrophy by the lability of the latter, with regression of hypertrophy after overload is removed. The increased LV wall thickness in elite athletes and racehorses regresses after deconditioning, whereas ventricular wall thickness in individuals with pathologic LV hypertrophy does not regress.
EFFECT OF TRAINING ON VALVULAR REGURGITATION
Athletic training influences function of the cardiac valves, and the prevalence of leaking cardiac valves (valvular regurgitation) is high in both human and equine athletes. When cardiac valves do not close sufficiently, blood flows backward in the cardiac chambers and is not available to working muscles or other vital organ systems. The grade of valvular regurgitation detected in racehorses is typically classified as small, and there is generally no progression in severity of regurgitation over time. These regurgitations often cannot be detected by auscultation but only by use of color Doppler echocardiography, which is a far more sensitive method. The increased prevalence of valvular regurgitation is seen in both human and equine athletes, and although the exact pathogenesis is unknown, it seems likely that altered loading conditions and morphologic and functional changes concurrent with cardiac hypertrophy are prerequisites for development of regurgitant valves.